From Beyond The Rainbow Somewhere

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Women retain and carry living DNA from every man with whom they have sexual intercourse, according to a new study by the University of Seattle and the Fred Hutchinson Cancer Research Center.

The study, which discovered the startling information by accident, was originally trying to determine if women who have been pregnant with a son might be more predisposed to certain neurological diseases that occur more frequently in males.

But as the scientists picked apart the female brain, the study began to veer wildly off course. As it turns out, the female brain is even more mysterious than we previously thought.

The study found that female brains often harbor “male microchimerism“, or in other words, the presence of male DNA that originated from another individual, and are genetically distinct from the cells that make up the rest of the woman.

According to the study: “63% of the females (37 of 59) tested harbored male microchimerism in the brain. Male microchimerism was present in multiple brain regions.”

So 63% of women carry male DNA cells that live in their brains. Obviously the researchers wanted to know where the male DNA came from.

Anyone care to guess? From the women’s fathers? No. Your father’s DNA combines with your mother’s to create your unique DNA. So where else could it come from?

Through the study the researchers assumed that the most likely answer was that all male DNA found living in the female brain came from a male pregnancy. That was the safe, politically correct assumption. But these researchers were living in denial.

Because when they autopsied the brains of women who had never even been pregnant, let alone with a male child, they STILL found male DNA cells prevalent in the female brain.

At this point the scientists didn’t know what the hell was going on. Confused, they did their best to hide the evidence until they could understand and explain it. They buried it in numerous sub studies and articles, but if you sift through them all you will find the damning statement, the one line that gives the game away and explains exactly where these male DNA cells come from.

What are they so afraid of?

“CONCLUSIONS: Male microchimerism was not infrequent in women without sons. Besides known pregnancies, other possible sources of male microchimerism include unrecognized spontaneous abortion, vanished male twin, an older brother transferred by the maternal circulation, or SEXUAL INTERCOURSE. Male microchimerism was significantly more frequent and levels were higher in women with induced abortion than in women with other pregnancy histories. Further studies are needed to determine specific origins of male microchimerism in women.“

So according to the scientists, the possible sources of the male DNA cells living in the women’s brains are:

an abortion the woman didn’t know about

a male twin that vanished

an older brother transferred by the maternal circulation

sexual intercourse

Considering the fact that 63% of women have male DNA cells residing in the recesses of their brain, which of the above possibilities do you think is the most likely origin of the male DNA?

The first three options apply to a very small percentage of women. They couldn’t possibly account for the 63% figure. The fourth option? It’s rather more common.

The answer is 4. Sex.

This has very important ramifications for women. Every male you absorb spermatazoa from becomes a living part of you for life. The women autopsied in this study were elderly. Some had been carrying the living male DNA inside them for well over 50 years.

Sperm is alive. It is living cells. When it is injected into you it swims and swims until it crashes headlong into a wall, and then it attaches and burrows into your flesh. If it’s in your mouth it swims and climbs into your nasal passages, inner ear, and behind your eyes. Then it digs in. It enters your blood stream and collects in your brain and spine.

Like something out of a scifi movie, it becomes a part of you and you can’t get rid of it.

We are only now beginning to understand the full power and ramifications of sexual intercourse.

“Immunotherapy marks an entirely different way of treating cancer — by targeting the immune system, not the tumor itself,”Sciencesaid in choosing this burgeoning field. Based on the idea that the immune system can be trained to attack tumors in the same way that it targets infectious agents, cancer immunotherapy exploits the ability to harness different types of immune cells circulating in the body.

A Rich History at Memorial Sloan-Kettering

Although cancer immunotherapy is being touted as a recent breakthrough in cancer treatment, its origins at Memorial Sloan-Kettering go back more than a century. In the 1890s, William Coley, a surgeon at New York Cancer Hospital (the predecessor to Memorial Sloan-Kettering) discovered cancer patients who suffered from infections after surgery often fared better than those who did not. His finding led to the development of Coley’s toxins, a cocktail of inactive bacteria injected into tumors that occasionally resulted in complete remission. But eventually the use of this treatment fell out of favor.

In the 1960s, research by Memorial Sloan-Kettering investigatorLloyd Oldled to the discovery of antibody receptors on the surface of cancer cells, which enabled the development of the first cancer vaccines and led to the understanding of how certain white blood cells, known as T cells or T lymphocytes, can be trained to recognize cancer.

Helping Patients Today

One of the pivotal milestones cited in the Science article is the work of immunologist James Allison in identifying a protein receptor on the surface of T cells called CTLA-4, which puts the brakes on T cells and prevents them carrying out immune attacks. He later identified an antibody that blocks CTLA-4 and showed that turning off those brakes allows T cells to destroy cancer in mice. (Dr. Allison, who spent nearly a decade of his career at Memorial Sloan-Kettering until last year, is now at MD Anderson Cancer Center in Houston.)

Dr. Wolchok’s research on immune therapies formelanomacontinues, includinga study earlier this yearthat found that more than half of patients with advanced skin melanoma experienced tumor shrinkage of more than 80 percent when given the combination of ipilimumab and the antibody drug nivolumab, another promising immunotherapy drug under investigation, suggesting that these two drugs may work better together than on their own.

The other major area of research highlighted in the Science story is the development of chimeric antigen receptor (CAR) therapy, based on the idea that a patient’s own immune cell type, called T cells, can be collected from blood, engineered to recognize cancer cells and acquire stronger antitumor properties, and reinfused to circulate through the bloodstream and attack those cancerous cells. Memorial Sloan-Kettering has been a leading center in developing this technology.

“This is a very exciting finding for patients with B cell ALL, directly borne out of our basic research on CARs for over a decade, and a landmark proof of concept in the field of targeted immunotherapy,” saysMichel Sadelain, Director of Memorial Sloan-Kettering’sCenter for Cell Engineering, who led the study, along with medical oncologistRenier Brentjens.

Memorial Sloan-Kettering continues to study this approach and now has clinical trials under way investigating it in other types of leukemia,lymphoma, andprostate cancer, with several more trials slated to begin soon.

Lung cancer is one of the most common and deadly types of cancer. Mouse models of lung cancer recapitulate many features of the human disease and have provided new insight about cancer development, progression and treatment. Now, a new study published by Cell Press in the September 13th issue of the journal Cancer Cell identifies protein signatures in mouse blood samples that reflect lung cancer biology in humans.

The research may lead to better monitoring of tumor progression as well as blood based early detection strategies for human lung cancer that could have a substantial impact on disease prognosis.

“In our study, we applied a comparative strategy of genetically engineered mouse models of cancer and integrated data at the genome and protein levels to uncover lung cancer signatures in blood samples that reflect different types of lung cancer, or that reflect signaling pathways driving tumor development,” says senior study author, Dr. Samir M. Hanash, from the Fred Hutchinson Cancer Research Center in Seattle. In order to identify blood protein signatures common to lung cancer, Dr. Hanash and colleagues looked at the proteins in the blood plasma of several different mouse lung tumor models and compared the proteins with those in models of other types of tumors.

The researchers identified individual protein signatures for molecularly distinct types of lung cancer and discovered that the networks of proteins provided insight into the genes that drive tumor development. Further, they identified proteins which were restricted to the blood samples from the lung cancer models and were not previously linked with lung cancer.

The authors went on to demonstrate the relevance of the protein signatures identified in the mouse models to human lung cancer. “We obtained evidence for concordant findings in human lung cancer cell lines and in plasmas collected from subjects with lung cancer at the time of diagnosis and in blood samples collected from asymptomatic subjects prior to diagnosis. These findings point to the power of integrating multiple types of studies and data to uncover lung cancer markers and may lead to early detection strategies for humans as well as strategies for monitoring tumor status in patients with the disease,” says Dr. Hanash.

These findings come from a study published online August 5 inJAMA Internal Medicine.

Women who had taken calcium-channel blockers for 10 years or more had more than double the usual risk for invasive ductal breast carcinoma (IDC) (odds ratio [OR], 2.4) and for invasive lobular breast carcinoma (ILC) (OR, 2.6). The researchers also observed a possible association between the long-term use of ACE inhibitors and reduced risks for both IDC (OR, 0.7) and ILC (OR, 0.6), although the risk estimate for IDC was within the limits of chance.

No Changes in Clinical Practice Recommended Yet

“We don’t think this should change clinical practice in any way. It was the first study of long-term antihypertensive use. It was an observational study, not a clinical trial. We can suggest an association, but we cannot infer any causal relation at this point,” lead author Christopher Li, MD, PhD, from the Fred Hutchinson Cancer Research Center in Seattle, told Medscape Medical News.

Dr. Li and colleagues interviewed women 55 to 74 years of age from the Puget Sound region — 880 with IDC, 1027 with ILC, and 856 without cancer (control group). Participants were interviewed in person to establish detailed histories of hypertension and heart disease and risk factors for cancer, including family history, obesity, smoking, and alcohol use. The researchers gathered data on the use of antihypertensive drugs, including beginning and end dates of use, drug names, dose, route of administration, pattern of use, and indication.

Calcium-channel blockers are among the most frequently prescribed medications in the United States; they accounted for nearly 98 million of the more than 678 million prescriptions filled in 2010.

Subjects who had used antihypertensives for 6 months or longer and were still using them were classified as current users, subjects who had used them for 6 months but were no longer using them were classified as former users, and subjects who had used them for less than 6 months were classified as short-term users.

“In examining duration effects for current users, we found an increased risk only in relation to the use of calcium-channel blockers for 10 years or longer, and an increased risk was observed for both IDC (OR, 2.4; 95% confidence interval [CI], 1.2 – 4.9; P = .04 for trend) and ILC (OR, 2.6; 95% CI, 1.3 – 5.3; P = .01 for trend). This association with 10 years or longer of current calcium-channel blocker use did not vary appreciably when results were further stratified by estrogen-receptor status,” the researchers report.

Dr. Li told Medscape Medical Newsthat they were surprised by the magnitude of the risk associated with calcium-channel blockers and by the decrease associated with ACE inhibitors.

“We expected that we might see some increase in breast cancer risk with calcium-channel blockers, but not a more than doubling of the risk,” Dr. Li said. “The suggestion of an association between ACE inhibitors and reduction in breast cancer risk was a very unexpected finding and is worthy of follow-up.”

The mechanism behind the apparent calcium-channel blocker effect is not known, Dr. Li explained, but some researchers suspect that these drugs might increase cancer risk by inhibiting apoptosis.

“First-Rate Study,” But Confirmation Needed

“The data are persuasive because this was a first-rate study: it was population-based, large (1900 case patients and 856 controls), identified cases from the Seattle-area SEER surveillance system, had a high (80%) case response rate, and used best practices in ascertaining medication use from study participants,” Patricia F. Coogan, ScD, from the Slone Epidemiology Center at Boston University, writes in a related commentary.

“Given these results, should the use of calcium-channel blockers be discontinued once a patient has taken them for 9.9 years? The answer is no, because these data are from an observational study, which cannot prove causality and by itself cannot make a case for change in clinical practice,” Dr. Coogan explains.

“If the 2- to 3-fold increase in risk found in this study is confirmed, long-term calcium-channel blocker use would take its place as one of the major modifiable risk factors for breast cancer. Thus it is important that efforts be made to replicate the findings,” Dr. Coogan notes.

“We are cautious and don’t want to read too much into this, since this was the first study to look at long-term use of these medications. We need to see confirmation of the study before making any clinical recommendations,” Dr. Li emphasized.

Those who treat patients with myelodysplastic syndromes (MDS) have been forced to become comfortable with a rather uncomfortable truth. MDS is a bone marrow failure syndrome that represents the most commonly diagnosed myeloid malignancy and predominantly affects older adults, with a median age at diagnosis of 71 years.1,2 The only cure for MDS is hematopoietic stem-cell transplantation (HSCT). For a variety of reasons, including patient comorbidities, availability of related or matched donors, related donor comorbidities, physician and patient preference, and treatment-related adverse events, transplantation is only considered in approximately 5% of patients with MDS.2 Thus, even when we offer disease-modifying therapies such as azacitidine, decitabine, and lenalidomide, we are ultimately palliating 95% of our patients.3–6Despite this, patients often perceive these drugs to have curative potential in this setting, but cure is unfortunately not possible with these agents.7

How do we change this paradigm? Although some factors, such as patient comorbidities and availability of donors, are largely immutable, others factors have improved, making HSCT more appealing. One such advance is reduced-intensity conditioning transplantation, which greatly reduces the toxicity of the preparative regimen without compromising efficacy, and in so doing has raised the age for potentially eligible transplantation candidates into the eighth decade.8 Another modifiable area is in identifying patients for whom the risk-benefit analysis for transplantation is more favorable compared with managing the disease with palliative intent. This, in turn, could affect patient and physician preferences.

In the article that accompanies this editorial, Koreth et al9 report on a Markov decision analysis exploring the role of reduced-intensity allogeneic HSCT in older patients with MDS. This statistical technique relies on assumptions, which themselves are based on best estimates of outcome given in previously published studies, to play out scenarios of what would happen in real life to a given patient if he or she decided to undergo HSCT early, at or near diagnosis, or instead to pursue supportive care, growth factor, or disease-modifying therapy. Although this approach is not perfect, it does allow for sensitivity analyses in which assumptions can be changed to see if the same conclusion holds, and it is the best substitute available in the absence of prospective, randomized studies. This is also not the first time some of these investigators have tackled this question, or this methodology. In 2004, Cutler et al10 published a decision analysis of patients with MDS treated with myeloablative conditioning transplantation. Given this conditioning regimen, patients were younger (with a median age of 40.4 years), and given the timing at which this analysis was conducted, a paucity of individual patient data were available to appropriately reflect nontransplantation treatment approaches. So, although the results of the study by Cutler et al make clinical sense, namely, that early transplantation provides maximal quality-adjusted survival in higher-risk patients with MDS (those falling into intermediate-2 and high-risk categories of the International Prognostic Scoring System [IPSS]), these conclusions have always given treating doctors pause because the participants did not reflect the full spectrum of patients with MDS who are seen in everyday clinical practice.

The analysis by Koreth et al9 addresses these shortcomings. Now, given the nonmyeloablative preparative regimen, the median age of the 132 patients undergoing transplantation gleaned from the Center for International Blood and Marrow Transplant Research, Dana-Farber Cancer Institute, and Fred Hutchinson Cancer Research Center data sets is 64 years—closer to what we see in clinic. Patients who did not undergo transplantation included 132 with lower-risk disease (IPSS low and intermediate-1) receiving best supportive care; 91 anemic or transfusion-dependent patients receiving erythropoiesis-stimulating agents; and 164 higher-risk patients with MDS receiving azacitidine or decitabine. Patients being treated with lenalidomide, immunosuppressive approaches, or drug combinations were not included. Primary end points of the model were life expectancy (LE) and quality-adjusted life expectancy, an end point adjusted for quality of life, the values of which were derived from studies in which patients may not reflect those included in the current analysis. The authors tried to keep the assumptions used in an already complicated model to a minimum, and in so doing ignored some real-life scenarios, such as a patient initially in the nontransplantation arm deciding at a later time to undergo transplantation. That being said, the results suggest that for lower-risk patients with MDS, median LE for those avoiding HSCT was approximately double that of those undergoing HSCT, at 77 versus 38 months. For higher-risk patients, a more modest advantage was seen for early HSCT, with a median LE of 36 months, versus 28 months for nontransplantation approaches. Interestingly, in the Kaplan-Meier survival curve, that advantage starts to become apparent only after 40 months of follow-up, when the therapy-related adverse effects of HSCT have been realized.

In a separate article accompanying this editorial, Voso et al11 report on a validation of the revised IPSS (IPSS-R) in a cohort of 380 patients with MDS who were registered in the Gruppo Romano Mielodisplasie and diagnosed over a 10-year period. The IPSS-R was developed to improve on what have been regarded as shortcomings of the classic IPSS, including both an underrepresentation and relative discounting of the importance of cytogenetic abnormalities, sensitivity to degrees of cytopenias, and weight given to blast percentage.12,13 The authors found that the IPSS-R was able to predict leukemia-free and overall survival in their population and that it was able to make these predictions better than the classic IPSS and WHO prognostic scoring system. This is not in itself novel—the initial publication of the IPSS-R included validation in a separate cohort from the Medical University of Vienna and demonstrated improved discriminatory capacity compared with the classic IPSS. However, this article does advance the field in showing the ability of the IPSS-R to retain its predictive abilities in a small cohort of patients treated with disease-modifying agents—a group not included in the development or validation of the IPSS-R previously. It remains to be seen whether the IPSS-R remains robust in larger cohorts of treated patients, or whether additional revisions to the IPSS-R may be required for treated patients as a group or for specific therapies. This task (determining whether further revisions are needed) is already being initiated by the International Working Group.

How can we apply these two publications to the next patient with an MDS who walks into clinic? In practice, the IPSS and IPSS-R are used both to predict survival and to help determine therapeutic approach. A patient falling into lower-risk categories is much more likely to be treated with erythropoiesis-stimulating agents, lenalidomide, immunosuppressants, or supportive care, whereas a higher-risk patient should be considered for hypomethylating agents or HSCT. The article by Voso et al11 helps refine our definition of lower and higher risk and starts to substantiate it in treated patients, whereas the article by Koreth et al9 adds further support to pursuing HSCT in higher-risk patients at presentation—as defined by the IPSS, not the IPSS-R. What remains are questions regarding the best approach for patients in the IPSS-R intermediate-risk category, who are neither lower nor higher risk, and the need to validate these approaches prospectively, given that our best data for most MDS management principles remain circumstantial. Unfortunately, there’s the rub.

Discovery has implications for development of a vaccine to prevent and treat HSV-2 and similar infections

Fred Hutchinson Cancer Research Center and University of Washington scientists have identified a class of immune cells that reside long-term in the genital skin and mucosa and are believed to be responsible for suppressing recurring outbreaks of genital herpes. These immune cells also play a role in suppressing symptoms of genital herpes, which is why most sufferers of the disease are asymptomatic when viral reactivations occur.

The discovery of this subtype of immune cells, called CD8αα+ T cells, opens a new avenue of research to develop a vaccine to prevent and treat herpes simplex virus type 2, or HSV-2. Identifying these T cells’ specific molecular targets, called epitopes, is the next step in developing a vaccine.

The findings are described in the May 8 advance online edition of Nature.

Better understanding of these newly identified CD8αα+ T cells may also play a critical role in developing effective vaccines against other types of skin and mucosal infections, according to senior author Larry Corey, M.D., an internationally renowned virologist and president and director of Fred Hutch.

“The discovery of this special class of cells that sit right at the nerve endings where HSV-2 is released into skin is changing how we think about HSV-2 and possible vaccines,” said Corey. “For the first time, we know the type of immune cells that the body uses to prevent outbreaks. We also know these cells are quite effective in containing most reactivations of HSV-2. If we can boost the effectiveness of these immune cells we are likely to be able to contain this infection at the point of attack and stop the virus from spreading in the first place. We’re excited about our discoveries because these cells might also prevent other types of viral infections, including HIV infection.”

There is currently no effective vaccine for genital herpes. “While antiviral treatment is available, the virus often breaks through this barrier and patients still can transmit the infection to others,” Corey said. “In addition, newborn herpes is one of the leading infections transmitted from mothers to children at the time of delivery. An effective genital herpes vaccine is needed to eliminate this complication of HSV-2 infection.”

The long-term persistence of CD8αα+ T cells where initial infection occurs may explain why patients have asymptomatic recurrences of genital herpes because these cells constantly recognize and eliminate the virus, according to Jia Zhu, Ph.D., corresponding author, research assistant professor in Laboratory Medicine at the University of Washington and an affiliate investigator in the Fred Hutch Vaccine and Infectious Disease Division.

“The cells we found perform immune surveillance and contain the virus in the key battlefield where infection occurs, which is the dermal-epidermal junction,” said Zhu. “These cells are persistent in the skin and represent a newly discovered phenotype distinguished from those of CD8+ T cells circulating in the blood.”

The dermal-epidermal junction (DEJ) is where the dermis (the tissue layers just beneath the skin) connects to the epidermis (outer skin layer). This junction is important because of the roles it plays in cellular communication, nutrient exchange and absorption, and other skin functions.

Scientists examined the DEJ for T cell activity because this is where the genital herpes virus multiplies after reactivating and traveling from its hiding place in the body’s sensory neurons. Previous research by the same research group showed that the nerve endings reach the dermal-epidermal junction and release the virus that infects the skin and can cause lesions.

Prior to this research, CD8αα+ T cells were known to exist in the gut mucosa. Much of the research on CD8+ T cells has focused on studying them in the circulating blood, which has a dominant phenotype of CD8αβ+. Fred Hutch and UW scientists compared the two types of CD8+ T cells and found that only the CD8αα+ T cells persist in the skin while CD8αβ+ T cells diminished from the tissue after healing of a herpes lesion.

“We did not expect to find CD8αα+ T cells in the skin,” Zhu said. “This was a surprise.”

The research involved using novel technologies to examine the T cells in human tissues. In all, the work provides a roadmap that can be applied to other human diseases, according to Zhu.

Zhu said the studies the research group performed in humans are unique. “To our knowledge, we are the only research group to use sequential human biopsies to study CD8+ T cell function in situ, in their natural spatial distribution and at their original physiological state,” she said.

According to the federal Centers for Disease Control and Prevention, 776,000 people in the United States are newly infected with herpes annually. Nationwide, 16.2 percent, or about one out of six people aged 14 to 49 years have genital HSV-2 infection. Generally, a person can only get HSV-2 infection during sexual contact with someone who has a genital HSV-2 infection. Transmission can occur from an infected partner who does not have a visible sore and may not know that he or she is infected.

Most individuals infected with HSV-2 or the related HSV-1, which causes genital herpes and cold sores, experience either no symptoms or have very mild symptoms that go unnoticed or are mistaken for another skin condition. Because of this, most people infected with HSV-2 are not aware of their infection.

Study also shows younger cancer patients are most vulnerable to financial stress

People diagnosed with cancer are more than two-and-a-half times more likely to declare bankruptcy than those without cancer, according to a new study from Fred Hutchinson Cancer Research Center. Researchers also found that younger cancer patients had two- to five-fold higher bankruptcy rates compared to older patients, and that overall bankruptcy filings increased as time passed following diagnosis.

The study, led by corresponding author Scott Ramsey, M.D., Ph.D., an internist and health economist at Fred Hutch, was published online on May 15 as a Web First in the journal Health Affairs. The article will also appear in the journal’s June edition.

Ramsey and colleagues, including a chief judge for a U.S. Bankruptcy Court, undertook the research because the relationship between receiving a cancer diagnosis and bankruptcy is less well understood than the much-studied link between high medical expenses and likelihood of bankruptcy filing.

“This study found strong evidence of a link between cancer diagnosis and increased risk of bankruptcy,” the authors wrote. “Although the risk of bankruptcy for cancer patients is relatively low in absolute terms, bankruptcy represents an extreme manifestation of what is probably a larger picture of economic hardship for cancer patients. Our study thus raises important questions about the factors underlying the relationship between cancer and financial hardship.”

For this study, researchers analyzed data from a population-wide registry of individuals over age 21 who lived in western Washington and who were diagnosed with cancer between Jan. 1, 1995 and Dec. 31, 2009. They were compared to a randomly sampled age-, sex-, and ZIP code-matched population of people without cancer. Cancer cases were identified using the Cancer Surveillance System of Western Washington, a population-based cancer registry based at Fred Hutch that is part of the National Cancer Institute’s Surveillance Epidemiology and End Results Program (SEER).

The cancer and control cohorts were both linked with the records of the U.S. Bankruptcy Court for the Western District of Washington. The court serves 19 counties in western Washington, including all 13 counties represented in the Cancer Surveillance System of Western Washington. Researchers included Chapter 7 or Chapter 13 bankruptcy filings only.

“This is the strongest evidence we have between a disease and risk for severe financial distress,” Ramsey said. “I’ve not seen other studies that linked databases of this quality.”

Ramsey directs the Hutchinson Institute for Cancer Outcomes Research (HICOR), which is dedicated to health economics and cancer outcomes research. Its mission is to improve the efficiency and effectiveness of cancer prevention, early detection and treatment to reduce the economic and human burdens of cancer. HICOR is believed to be the first of its kind among comprehensive cancer centers nationwide.

Among the study’s key findings:

Between 1995 and 2009 there were 197,840 people in western Washington who were diagnosed with cancer and met the inclusion criteria for the study. Of those, 4,408 (2.2 percent) filed for bankruptcy protection after diagnosis. Of the matched controls who were not diagnosed with cancer, 2,291 (1.1 percent) filed for bankruptcy.

Compared to cancer patients who did not file for bankruptcy, those who did were more likely to be younger, female and nonwhite. The youngest age groups had up to 10 times the bankruptcy rate as compared to the older age groups. The authors noted that because cancer is generally a sudden and unexpected event, the risk of bankruptcy is influenced by factors such as debt load before diagnosis, assets, presence and terms of health and disability insurance, number of dependent children, and incomes of others in the household at the time of the cancer diagnosis.

“The youngest groups in the study were diagnosed at a time when their debt-to-income ratios are typically highest — often unavoidably, because they are paying off student loans, purchasing a home, or starting a business,” the authors wrote. “All working-age people who develop cancer face loss of income and, in many cases, loss of employer-sponsored insurance, both of which can be devastating for households in which the patient is the primary wage earner.”

In contrast, people age 65 or older generally have Medicare insurance and Social Security benefits. These older people are likely to have more assets and possibly more income than working-age people. “However, it is likely that having stable insurance (specifically, coverage not tied to employment) plays a major role in mitigating the risk of bankruptcy for those over age sixty-five,” the authors wrote.

The proportion of cancer patients who filed for bankruptcy within one year of diagnosis was 0.52 percent, compared to 0.16 percent within one year for the control group. For bankruptcy filings within five years of diagnosis, the proportion of cancer patients was about 1.7 percent, compared to 0.7 percent for the control group.

The incidence rates for bankruptcy at one year after diagnosis for the cancers with the highest overall incidence rates, stated as rates per 1,000 person years from diagnosis, were as follows: thyroid, 9.3; lung, 9.1; uterine, 6.8; leukemia/lymphoma, 6.2; colorectal, 5.9; melanoma, 5.7; breast, 5.7; and prostate. 3.7. The incidence rate for all cancers combined was 6.1. (Person-years takes into account the number of people in the study and the amount of time each person spent in the study.)

The high bankruptcy incidence rate for those with thyroid cancer may be because thyroid cancer affects younger women more often than other cancers do according to the researchers. “Compared to men, younger women are more likely to live in single-income households and to have lower wages and lower rates of employment, and therefore less access to high-quality health insurance – leaving them more financially vulnerable,” the authors wrote.

Men who take statins are less likely to die from prostate cancer than those who don’t

– Men with prostate cancer who take cholesterol-lowering drugs called statins are significantly less likely to die from their cancer than men who don’t take such medication, according to study led by researchers at Fred Hutchinson Cancer Research Center. The findings are published online today in The Prostate.

The study, led by Janet L. Stanford, Ph.D., co-director of the Prostate Cancer Research Program and a member of the Hutchinson Center’s Public Health Sciences Division, followed about 1,000 Seattle-area prostate cancer patients. Approximately 30 percent of the study participants reported using statin drugs to control their cholesterol. After a mean follow-up of almost eight years, the researchers found that the risk of death from prostate cancer among statin users was 1 percent as compared to 5 percent for nonusers.

“If the results of our study are validated in other patient cohorts with extended follow-up for cause-specific death, an intervention trial of statin drugs in prostate cancer patients may be justified,” Stanford said.

“While statin drugs are relatively well tolerated with a low frequency of serious side effects, they cannot be recommended for the prevention of prostate cancer-related death until a preventive effect on mortality from prostate cancer has been demonstrated in a large, randomized, placebo-controlled clinical trial,” said first author Milan S. Geybels, M.Sc., formerly a researcher in Stanford’s group who is now based at Maastricht University in The Netherlands.

The study is unique in that most prior research of the impact of statin use on prostate cancer outcomes has focused on biochemical recurrence – a rising PSA level – and not prostate cancer-specific mortality. “Very few studies of statin use in relation to death from prostate cancer have been conducted, possibly because such analyses require much longer follow-up for the assessment of this prostate cancer outcome,” Geybels said.

The potential biological explanation behind the association between statin use and decreased mortality from prostate cancer may be related to cholesterol- and non-cholesterol-mediated mechanisms.

An example of the former: When cholesterol is incorporated into cell membranes, these “cholesterol-rich domains” play a key role in controlling pathways associated with survival of prostate cancer cells.

An example of the latter: Statin drugs inhibit an essential precursor to cholesterol production called mevalonate. Lower levels of mevalonate may reduce the risk of fatal prostate cancer.

“Prostate cancer is an interesting disease for which secondary prevention, or preventing poor long-term patient outcomes, should be considered because it is the most common cancer among men in developed countries and the second leading cause of cancer-related deaths,” Geybels said. “While many prostate cancer patients have indolent, slow-growing tumors, others have aggressive tumors that may recur or progress to a life-threatening disease despite initial therapy with radiation or surgery. Therefore, any compound that could stop or slow the progression of prostate cancer would be beneficial,” he said.

However, breast cancer survivors who consume alcohol in moderation may have a reduced risk of dying from heart disease

Although previous research has linked alcohol consumption to an increased risk of developing breast cancer, a new study has found that drinking before and after diagnosis does not impact survival from the disease. In fact, a modest survival benefit was found in women who were moderate drinkers before and after diagnosis due to a reduced risk of dying from cardiovascular disease, a major cause of mortality among breast cancer survivors.

“Our findings should be reassuring to women who have breast cancer because their past experience consuming alcohol is unlikely to impact their survival after diagnosis,” said Newcomb. “This study also provides additional support for the beneficial effect of moderate alcohol consumption with respect to cardiovascular disease.”

The study was based on data from almost 23,000 women with breast cancer who participated in theCollaborative Breast Cancer Study, a National Cancer Institute-sponsored, multi-site, population-based study of risk factors for breast cancer, and the largest such study of its kind. The study began in 1988 and was conducted in New Hampshire, Massachusetts and Wisconsin. In a smaller follow-up study between 1998 and 2001, about 5,000 study participants with breast cancer were also sent a follow-up questionnaire about their alcohol consumption habits after diagnosis.

Among study participants with a history of breast cancer, the authors found that the amount and type of alcohol a woman reported consuming in the years before her diagnosis was not associated with her likelihood from dying from breast cancer. However, the authors also found that those who consumed a moderate level of alcohol (three to six drinks per week) in the years before their cancer diagnosis were 15 percent less likely to die from cardiovascular disease than non-drinkers. Moderate wine consumption in particular was associated with a lower risk of cardiovascular disease mortality, while no such benefit was evident for consumption of beer or spirits, or for heavier levels of alcohol consumption.

Similar patterns were evident when considering reported alcohol consumption after breast cancer diagnosis. The amount and type of alcohol a woman consumed after diagnosis did not appear to be associated with survival of breast cancer, but those who consumed alcohol in moderation experienced a 40- to 50-percent lower mortality rate from cardiovascular disease.

What could account for the difference in alcohol’s impact on developing breast cancer risk and on survival from the disease? “It could be that the kind of breast cancer that is more likely to be diagnosed among women who drink may be more responsive to hormone-modifying therapies,” Newcomb said. Alcohol consumption is believed to influence breast cancer risk through increases in estrogen production in both pre- and post-menopausal women.

Ever since chemotherapy was introduced into the practice of western medicine, doctors and oncologists have been trying to answer this nagging question: Why does chemotherapy seem to work at first, but then cancer tumors cells grow back even more aggressively while the body becomes resistant to chemotherapy?

It turns out that chemotherapy damages healthy cells, causing them to secrete a protein that accelerates the growth of cancer tumours.

This protein, dubbed “WNT16B,” is taken up by nearby cancer cells, causing them to “grow, invade, and importantly, resist subsequent therapy,” said Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattle. He’s the co-author of the study that documented this phenomenon, published in Nature Medicine.

The findings of the study were confirmed with prostate cancer, breast cancer and ovarian cancer tumors. This discovery that chemotherapy backfires by accelerating cancer tumor growth is being characterized as “completely unexpected” by scientists.

The chemotherapy fraud exposed

As NaturalNews has explained over the last decade, chemotherapy is medical fraud. Rather than boosting the immune response of patients, it harms the immune system, causing tumors to grow back. This latest researching further confirms what we’ve known for years in the holistic health community: That chemotherapy is, flatly stated, poison. It’s not “treatment,” it’s not medicine, and it’s not prevention or a cure. It’s poison with virtually no medicinal value except in perhaps one to two percent of cancer cases.

The No. 1 side effect of chemotherapy is, by the way, cancer. Cancer centers should technically be renamed “poison centers” because they are in the business of poisoning patients with a toxic cocktail of chemicals that modern science reveals to be a cancer tumor growth accelerant!